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Residential exposure to estrogen disrupting hazardous air pollutants and breast cancer risk: the California Teachers Study.

ABSTRACT: BACKGROUND:Some studies show increased breast cancer risk from exposure to xenoestrogens, but few have explored exposures via ambient air, which could impact large populations. OBJECTIVES:This study explored the association between breast cancer risk and residential exposures to ambient estrogen disruptors among participants in a large cohort study, the California Teachers Study. METHODS:Participants consisted of 112,379 women free of breast cancer and living at a California address in 1995/1996. Eleven hazardous air pollutants from the US Environmental Protection Agency 2002 list were identified as estrogen disruptors based on published endocrine disrupting chemical lists and literature review. Census-tract estrogen disruptor air concentrations modeled by the US Environmental Protection Agency in 2002 were assigned to participants' baseline addresses. Cox proportional hazards models were used to estimate hazard ratios associated with exposure to each estrogen disruptor and a summary measure of nine estrogenic hazardous air pollutants among all participants and selected subgroups, adjusting for age, race/birthplace, socioeconomic status, and known breast cancer risk factors. RESULTS:Five thousand three hundred sixty-one invasive breast cancer cases were identified between 1995 and 2010. No associations were found between residential exposure to ambient estrogen disruptors and overall breast cancer risk or hormone receptor-positive breast cancer risk, nor among targeted subgroups of participants (pre-/peri-menopausal women, post-menopausal women, never-smokers, non-movers, and never-smoking non-movers). However, elevated risks for hormone receptor-negative tumors were observed for higher exposure to cadmium compounds and possibly inorganic arsenic among never-smoking non-movers. CONCLUSION:Long-term, low-dose exposure to ambient cadmium compounds or possibly inorganic arsenic may be a risk factor for breast cancer.

SUBMITTER: Liu R

PROVIDER: S-EPMC5101045 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature

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Residential exposure to estrogen disrupting hazardous air pollutants and breast cancer risk: the California Teachers Study.

Liu Ruiling R Nelson David O DO Hurley Susan S Hertz Andrew A Reynolds Peggy P

Epidemiology (Cambridge, Mass.) 20150501 3

<h4>Background</h4>Some studies show increased breast cancer risk from exposure to xenoestrogens, but few have explored exposures via ambient air, which could impact large populations.<h4>Objectives</h4>This study explored the association between breast cancer risk and residential exposures to ambient estrogen disruptors among participants in a large cohort study, the California Teachers Study.<h4>Methods</h4>Participants consisted of 112,379 women free of breast cancer and living at a Californi ...[more]

PMID: 25760782

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Project description:BackgroundStudies suggest that higher breast cancer rates in urban areas persist after accounting for the prevalence of known risk factors, leading to speculation that urban environmental exposures, such as air pollution, may play a role in the etiology of breast cancer. Combining modeled ambient air concentrations with data from a large prospective cohort of California women with over 15 years of follow-up, we examined the relationship between breast cancer incidence and modeled concentrations of air pollutants shown to be mammary gland carcinogens (MGCs).MethodsThe study population of 112,378 California Teachers Study participants included 5,676 women diagnosed with invasive breast cancer. Modeled annual average ambient air concentrations of 24 MGCs from the U.S. Environmental Protection Agency were linked to participants' addresses. Cox proportional hazards models were used to estimate hazard rate ratios and 95% confidence intervals associated with residential MGC levels. MGCs were examined individually and as a combined summary variable for all participants, in selected subsets, and by tumor hormone responsiveness.ResultsInitial models yielded some evidence for increased risk for several compounds, including acrylamide, carbon tetrachloride, chloroprene, 4,4'-methylene bis(2-chloroaniline), propylene oxide, and vinyl chloride, but after adjustment for multiple comparisons, only results for propylene oxide and vinyl chloride remained statistically significant. In subset analyses, estrogen-receptor positive or progesterone-receptor positive (ER+/PR+) tumors were associated with higher ambient levels of acrylamide, benzidine, carbon tetrachloride, ethylidene dichloride, and vinyl chloride, while ER-/PR- tumors were associated with higher ambient levels of benzene. Interesting results for different compounds were observed within certain subsets of the population.ConclusionWhile our initial models yielded several elevated risk estimates, after adjusting for multiple comparisons and breast cancer risk factors, most hazard ratios were no longer statistically significant. Our subset analyses, however, suggest that elevated risk may be associated with some compounds for certain subgroups of interest. A summary variable for all 24 MGCs did not offer any advantage over the models for individual compounds. Results must be interpreted cautiously, as estimated exposure was limited to modeled annual average ambient air concentrations, and could not account for other sources or routes other than inhalation.

Project description:BackgroundStudies of effects of air pollution on gestational diabetes mellitus (GDM) have not been consistent, and there has been little investigation of effects of exposure preceding pregnancy. In previous studies, the temporal relationship between exposure and GDM onset has been difficult to establish.MethodsData were obtained for 239,574 pregnancies between 1999 and 2009 in a population-based health care system with comprehensive electronic medical records. Concentrations of ambient nitrogen dioxide (NO2), particulate matter (PM) ≤2.5 μm in aerodynamic diameter (PM2.5) and ≤10 μm (PM10), and ozone (O3) during preconception and the first trimester of pregnancy at the residential birth address were estimated from regulatory air monitoring stations. Odds ratios (ORs) of GDM diagnosed in the second and third trimesters in association with pollutant exposure were estimated using generalized estimating equation models adjusted for birth year, medical center service areas, maternal age, race/ethnicity, education, census-tract household income, and parity.ResultsIn single-pollutant models, preconception NO2 was associated with increased risk of GDM (OR = 1.10 per 10.4 ppb, 95% confidence interval [CI]: 1.07, 1.13). First trimester NO2 was weakly associated with GDM, and this was not statistically significant (OR = 1.02 per 10.4 ppb, 95% CI: 0.99, 1.05). Preconception NO2 associations were robust in multi-pollutant models adjusted for first trimester NO2 with another co-pollutant from both exposure windows. In single-pollutant models, preconception PM2.5 and PM10 associations were associated with increased risk of GDM (OR = 1.04 per 6.5 μg/m3, 95% CI: 1.01, 1.06; OR = 1.03 per 16.1 μg/m3, 95% CI: 1.00, 1.06, respectively), but these effect estimates were not robust to adjustment for other pollutants. In single-pollutant models, preconception and first trimester O3 were associated with reduced risk of GDM (OR = 0.94 per 15.7 ppb, 95% CI: 0.92, 0.95; OR = 0.95 per 15.7 ppb, 95% CI: 0.94, 0.97), associations that were robust to adjustment for co-pollutants.ConclusionsMaternal exposure to NO2 during the preconception trimester may increase risk of GDM.

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Residential exposure to estrogen disrupting hazardous air pollutants and breast cancer risk: the California Teachers Study.

Publications

Residential exposure to estrogen disrupting hazardous air pollutants and breast cancer risk: the California Teachers Study.

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